ZHX2 controls HIF1α oncogenic signaling and tumorigenesis in triple-negative breast cancer.

Stereotactic body radiotherapy combined with immunotherapy and chemotherapy in neoadjuvant setting exhibited a promising anti-tumor activity and an acceptable safety profile in triple-negative breast cancer patients.

The upregulation of TLN1 contributes to the metastasis of triple-negative breast cancer (TNBC), and a small-molecule C67399 was screened for blocking TLN1 and integrin β1 may hold promise for the treatment of TNBC.

A microfluidic device induces doxorubicin-resistant polyaneuploid cancer cells from triple negative breast cancer cells, revealing NUPR1/HDAC11 axis dysfunction drives chemoresistance, increasing tumor heterogeneity and impacting clinical outcomes.

Machine learning-assisted experiments reveal CD81 as a novel binding partner of CD44 in driving cancer stemness, tumor cell clustering, and extracellular vesicle integrity in human and mouse breast cancer.

Anomalous expression of the testis protein ZNF165 in cancer cells promotes assembly of a neomorphic transcriptional complex that modulates transcription of TGFβ target genes to support tumor cell survival.

A peptide motif targeting tumor-infiltrating macrophage in triple-negative breast cancer delays tumor growth and favors an antitumor immune response.

TNFAIP2 was found to interact with IQGAP1 and Integrin β4, which activates RAC1 through TNFAIP2 and IQGAP1 and confers DNA damage-related drug resistance in triple-negative breast cancer.

ctDNA predict prognosis and treatment response of mTNBC patients more sensitively than traditional tumor markers, which implies ctDNA may be valuable for individualized treatment decision-making and paves the way for a non-invasive real-time clinical management strategy in patients with mTNBC.

Identification of a pro-tumorigenic and pro-metastatic role of EHD2 protein in triple-negative breast cancer (TNBC) through the store-operated calcium entry (SOCE) pathway provides a rationale for potential targeting of EHD2-overexpressing TNBC with SOCE inhibitors.